In 1977 a flu broke out in northeast China which eventually spread to Russia and then around the world. It eventually took the lives of approximately 700,000 people around the world most of whom were young. It came to be known as the “Russian flu” because Russia was the first country to report it to the WHO. Scientists who examined its DNA concluded it was nearly identical to a previous strain of the flu virus which had caused an outbreak between 1949 and 1950.
In nature, the flu doesn’t remain unchanged for 27 years as it circulates. So the fact that the “Russian flu” was nearly identical to the earlier strain eventually led to the conclusion that the Russian flu was likely the result of a lab leak or possibly a failed attempt to inoculate people with live attenuated virus.
In a research paper published in the journal Nature in 1978, a team of scientists from The City University of New York found that the 1977 virus was genomically similar to the 1950 virus — almost as though the viral evolution had been frozen in time.
It may be possible for an accidental mutation to develop that is similar to a variant from the past — but the scientists deemed it was not plausible to speculate that such back mutations accidentally produced a strain so similar to something that circulated 27 years ago.
This next bit is pretty striking in light of current events:
A 1978 study by researchers from the Chinese Academy of Medical Sciences showed that the virus primarily affected those below the age of 20 — giving support to the theory that those above that age had already been exposed to the same virus before, and thus had developed immunity.
In the same paper, however, the team dismissed the lab leak theory in one sentence, stating that none of the “laboratories concerned” had been storing or working with the H1N1 for a long time.
But as this 2015 paper explains, a lab leak (or alternatively a failed immunization effort with live attenuated virus) is now considered the most likely explanation for the Russian flu as alternate explanations have been found to be unconvincing. Again, see if this doesn’t sound familiar:
A biosafety lapse in a research laboratory is now most often cited as the cause of the 1977-1978 reemergence of the H1N1 influenza virus strain (Fig. 2). The evidence in favor of this possibility is the clear unnatural origin of the virus and its temperature sensitivity, suggesting laboratory manipulations. At the time of the epidemic, however, the World Health Organization excluded the lab accident possibility after discussions with influenza virus laboratory researchers in the Soviet Union and China, finding that “the laboratories concerned either had never kept H1N1 virus or had not worked with it for a long time”
There’s a graphic showing how various theories have been proposed and discussed by researchers over the years. Since about 2008, the lab leak seems to be the dominant explanation:
But the author of the paper seems to think it’s more likely the release was the result of a vaccine trial using live attenuated virus which wasn’t sufficiently attenuated.
There are two factors that point to the 1977 epidemic as resulting from vaccine challenge or trials: (i) live attenuated influenza virus (LAIV) research was extensive at the time, and (ii) a 1976 H1N1 swine flu outbreak was feared to have pandemic potential and led to a resurgent interest in H1N1 protection and research (12).
Between 1962 and 1973, almost 40,000 children participated in eight LAIV trials in the USSR (13). Scientists at the Peking Vaccine and Serum Institute in China also carried out clinical trials using live vaccines during the same time period (1). Additionally, there are records of the mass production of a live H1N1 vaccine in Odessa, USSR, in 1977 (14, 15). In the early days of research in the 1940s, LAIVs were often able to regain virulence upon administration to humans and cause disease (16). In addition, many strains isolated from the 1977 outbreak (for example, the A/Tientsin/78/77 isolate) were temperature sensitive (ts), meaning that the virus could not replicate at higher temperatures. Temperature sensitivity generally occurs only after a series of laboratory manipulations, typical in generation of LAIVs, and is used as a biological marker of attenuation. While not all of the 1977-1978 strains were temperature sensitive, a comparison of all 1977 strains shows a higher prevalence of the ts phenotype than in 1950 strains, supporting the claim that the outbreak may have resulted from attempts at attenuation for vaccine purposes (1, 17).
Whatever the exact cause, most experts now believe that the “Russian flu” of 1977 was caused by a virus which had been collected sometime around 1950, worked on in a lab and then essentially released back into the world by accident. The Russians and the Chinese denied having done any such thing and the WHO supported those denials at the time, but three decades later most scientists now believe the denials must be false. Flu viruses simply don’t hibernate for 27 years and then suddenly cause an outbreak in an unchanged form.